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Notes: Abstract This investigation developed an experimental design that (1) detailed the distribution of A. actinomycetemcomitans in Subgingival plaque related to the level of serum antibody to this pathogen; (2) used broad based subgingival plaque sampling to allow a definition of the distribution of A. actinomycetemcomitans infection in periodontitis patients; (3) described the distribution of A. actinomycetemcomitans serotypes in patients and within sites; and, (4) assessed how this infection impacted upon local clinical symptoms of disease. We noted a significant positive relationship between the level of IgG anti-A. actinomycetemcomitans antibody and the frequency of teeth infected until nearly 13 teeth demonstrated an infection. Furthermore, the results showed a generally negative relationship between the antibody level and the burden of A. actinomycetemcomitans in the infected sites. Interproximal sites associated with first molar teeth were the predominant sites for subgingival colonization; incisors were also frequently infected in this population. The first molar teeth also exhibited the greatest level of A. actinomycetemcomitans while the incisors demonstrated a high level of A. actinomycetemcomitans in individual sites. The results clearly indicated the majority of the sites sampled were colonized by a single serotype of A. actinomycetemcomitans. We detected A. actinomycetemcomitans nearly 2 × times more frequently and a significant increase in the proportion of A. actinomycetemcomitans was found in samples obtained from teeth with bleeding on probing. The results also showed a significant trend for both pocket depth and attachment levels to be related to the presence and proportion of A. actinomycetemcomitans in the subgingival plaque. These findings detail the microbiological, immunological and clinical characteristics of a unique subset of periodontitis patients that appear to exhibit disease associated (caused?) with A. actinomycetemcomitans infection irrespective of clinical categorization. The results support a unique distribution of this microorganism in the subgingival ecology that is related to active host immune responses and clinical presentation of the tooth.

Notes: Abstract 27 subjects with active destructive periodontal diseases were treated by modified Widman flap surgery and systemic tetracycline and divided into 4 groups based on pre- and post-therapy hazard rates (% of sites losing 〉 3 mm of attachment in 1 year). Pre- and post-therapy hazard rates were respectively: group T (3 subjects) 〈 4 and 〈 4; group II (8 subjects) 〉 4 and 〈 4; group III (3 subjects) 〈 4 and 〉 4; group IV (refractory group of 13 subjects) 〉 4 and 〉 4. Baseline mean pocket depths and attachment loss of groups 1 and II subjects were less than groups III and IV subjects and exhibited less suppuration. 6 group IV subjects lost a total of 38 teeth after therapy, in contrast to no tooth loss in subjects in the other 3 groups. Redness, bleeding on probing, plaque levels and age did not differ among groups. Subjects in the 4 groups differed in the subgingival species to which they showed elevated serum antibody responses. Group IV subjects showed elevated responses to a select range of gram-negative species, including A. actinomycetemcomitans strains Y4 or ATCC 29523, F. nucleatum and B. intermedius. No subject in any of the other groups exhibited an elevated response to B. intermedius. The mean % of each species in all sampled sites, both before and after therapy, was computed for each subject. Subjects in groups III and IV (high post-therapy hazard rates) exhibited elevated mean levels of B. forsythus, F. nucleatum, S. intermedius, E. corrodens, and B. gingivalis. Groups I and II subjects showed elevated mean levels of an unnamed Actinomyces species. Refractory subjects (group IV) did not constitute a homogeneous group. While subjects in this group had higher levels of pathogens, it appeared that they differed in the combinations of predominant species. 3 major microbial complexes were observed: (1) B. forsythus, F. nucleatum and W. recta (3 subjects); (2) S. intermedius, B. gingivalis and P. micros (3 subjects); (3) S. intermedius and F nucleatum (7 subjects) with or without B. gingivalis.

Notes: Abstract Clinical, microbiological and immunological factors were examined using data from a subject with periodontosis. The subject was monitored at bimonthly intervals for 26 months at 6 sites per tooth for redness, plaque, suppuration, bleeding on probing, pocket depth, and attachment level. Using attachment level measurements and the tolerance method of analysis, sites with active disease and control (inactive) sites of equal pocket depth were selected. Subgingival plaque samples were taken from these sites for predominant cultivable and dark field evaluation before, and 5 and 13 months after treatment by Widman flap surgery and systemic tetracycline. 50 isolates from each of 5 sites monitored before and after treatment were characterized and, if possible, identified. Active sites showed between 2 and 6 mm of attachment loss prior to therapy and “gained” between 2 and 9 mm of attachment after therapy. The control sites “gained” 0 to 1 mm of attachment after therapy. Bleeding on probing was significantly reduced after treatment, whereas plaque accumulation increased significantly in the sampled sites. Similar changes were seen in the remaining sites.The proportions of Actinobacillus actinomycetemcomitans and Selenomonas sputigena were elevated in active sites, while proportions of Bacleroides intermedius were elevated in control sites. 5 months after treatment, proportions of A. actinomycetemcomitans, S. sputigena and Eikenella corrodens were significantly decreased in the previously active sites and proportions of B. intermedius and E. corrodens were significantly decreased in the control sites. 13 months after therapy, the proportions of Fusobacterium nucleatum and Capnocytophaga species had increased.Multiple linear regression analysis was used to examine models which could “predict” the outcome, attachment level change in the previous monitoring period. The proportions of A. actinomycetemcomitans and S. sputigena, which were associated with destruction, coupled with the proportions of Streptococcus sanguis II and Campylobacter concisus which were associated with “gain” could predict prior attachment level change with an r2 of 0.93.Humoral antibody response to A. actinomycetemcomitans and C. sputigena significantly increased in a period in which multiple actively breaking down sites were detected. Antibody responses to 20 other species tested did not significantly change during the course of monitoring. Crevicular fluid and tissue levels of antibody to A. actinomycetemcomitans were elevated in 5 of 6 active destructive lesions prior to therapy. Surgical and tetracycline therapy diminished the local antibody response to A. actinomycetemcomitans to levels found in serum.

Notes: Abstract Data derived from periodontitis patients have provided support for a relationship between the distribution of selected members of the periodontopathic microbiota and antibody levels to the intact bacteria in both serum and GCE These data are consistent with the systemic antibody as a reflection of the host response to an infectious process associated with an episode of disease activity. The purpose of this report is to address the concept that the host antibody responses may help to elucidate the specific etiologic agents and be used to model the risk for future periodontal disease progression in recurring periodontitis. These findings from one study in adult periodontitis patients indicated that elevations in certain antibody specificities are most closely associated with patients exhibiting a risk of disease recurrence. Furthermore, analysis of the frequency of antibody elevations suggested that patients capable of maintaining elevated antibody to these pathogens past–treatment, may be indicative of an individual at less risk. A 2nd investigation was implemented to address questions concerning host–parasite interactions in A. actinomycetemcomitans–associated recurring periodontitis. The results showed distinctive characteristics of local and systemic antibody responses and A. actinomycetemcomitans infection in patients with varying extents of recurrent disease. These longitudinal studies developed evidence for the potential of local and/or systemic antibody responses as indicators of periodontal disease recurrence.

Notes: Abstract Clinical syndromes of 22 untreated patients with advanced destructive periodontal disease were analyzed using cluster analysis. Clinical characteristics coded for each patient included age, sex, measures of gingival inflammation, plaque, suppuration, pocket depth, attachment level, extent and pattern of bone loss, rate of change in pocket depth, and correlation coefficients between certain clinical measurements. Microbiologic features included darkfield enumeration of 10 morphologically distinct forms of organisms which were removed from the three sites showing the most advanced destruction in each patient, as well as viable counts of specific microbial groups from the same teeth using elective and selective media. Serum antibody levels were determined by the ELISA technique to 13 species of subgingival microorganisms. The Gower coefficient was used to estimate similarity between patients and clusters were formed using an average unweighted linkage sort. Three distinct patient clusters were observed with greater than 70 % average intra-cluster similarity. One subject did not fall into any of the patient clusters. The features which defined and differentiated the clusters were found to include age of subject, extent and patterns of bone loss, percent of sites showing change in pocket depth and attachment level, percent of small motile rods, intermediate spirochetes and fusiforms and serum IgG levels against Bacteroides gingivalis, Selenomonas sputigena and a Wolinella strain.

Notes: Abstract 76 subjects with prior evidence of destructive periodontal diseases were monitored clinically and immunologically every 2 months for up to 5 years. Clinical parameters measured included bleeding on probing, gingival redness. plaque accumulation, suppuration, pocket depth and attachment level. Blood samples were taken by venipuncture and serum antibody levels to a series of 18 subgingival species determined. 33 of these subjects showed evidence of active disease during the monitoring period, based on changes in attachment level measurements assessed using the tolerance method of analysis. Mean attachment loss in these 33 subjects varied from 1.4 mm to 9.0 (median value 3.4 mm) and subjects whose mean attachment level was above the median showed a higher % of pockets 〉 3 mm and more suppuration. Severity of gingival inflammation related poorly to mean attachment loss. Subgingival plaque samples were taken from the active site(s) and from control sites of equal pocket depth and attachment loss in the same active disease subjects, prior to therapy, for predominant cultivable microbiota studies. 50 randomly selected isolates were identified from each sample. Predominant cultivable species in 170 pretreatment active and inactive sites combined (8500 isolates) were enumerated. The most frequently detected species were F. nucleatum (112 sites) and S. intermedius (106 sites), although the predominant species in the samples from each subject differed. The distribution of putative pathogens differed among subjects. For example. A. actinomycetemcomitans was found in 21 samples in 11 subjects and B. forsythus was found in 18 samples from 10 individuals. Antibody response patterns to the 18 subgingival species also varied among subjects. More than 81% (26/32) of the subjects demonstrated a mean elevated serum antibody level to at least 1 micro-organism, while I subject showed an elevated response to 5 species. No pattern(s) of elevated antibody response(s) could be related to severity of attachment loss. Collectively, the data suggest that clinically, immunologically and microbiologically distinctive destructive periodontal diseases exist, and appropriate classifications could be devised.

Notes: Abstract. Serum antibody specificity to oral micro-organisms was used to delineate the pathogens associated with early-onset periodontal diseases in a Turkish population. Additionally, comparison of the findings to those derived from a clinically similar US patient population described differences in bacterial specific antibody between these 2 geographic regions. Serum from 89 (LJP), 86 (RPP) and 94 (normal) subjects was analyzed (ELISA) to determine IgG antibody to 14 oral micro-organisms. All LJP patients from Turkey exhibited elevated antibody levels to A. actinomycetemcomitans (serotypes c and a significantly increased), while antibody levels to A. actinomycetemcomitans Y4 and JP2 (serotype b) were significantly higher in US LJP patients. 50% of the Turkish RPP patients also showed elevated anti-A. actinomycetemeomitans antibody, although the US RPP patients exhibited significantly higher antibody levels and frequency of elevated antibody to the A. actinomycetemcomitans serotypes. Healthy subjects and LJP and RPP patients from the US exhibited higher antibody levels to all 3 P. gingivalis serogroups compared to those from Turkey, although, the frequency of elevated antibody to the P. gingivalis serogroups was significantly higher in LJP and RPP patients from Turkey than from the US. Interestingly, 87% and 77% of the LJP patients in the Turkish population had elevated antibody responses to P. gingivalis and E. corrodens, respectively, which was not observed in the US LJP patients. These data suggested that considerable variation exists in the systemic antibody levels to periodontopathogens between these 2 countries. This supports potential differences in subgingival colonization or antigenic composition of these pathogens between patient populations from different geographical regions.

Notes: Studies were initiated to investigate the antigenic relationship among oral species of Bacteroides. Antigenic differences among the Bacteroides were assessed with an ELISA using antisera from immunized rabbits and sera obtained from subjects with periodontal disease. Multiple species of Bacteroides were examined, including: B. gingivalis, 2 homology groups of B. intermedius, B. melaninogenicus, B. denticola, B. loescheii, B. oralis, B. levii, B. gracilis, B. buccae. and B. corporis. Both rabbit and human sera reacted with distinct surface antigenic determinants in each of the species of Bacteroides. Additional relationships were defined, such that the 2 homology groups of B. intermedius exhibited a similarity of approximately 30–40%, while the B. melaninogenicus and B. loescheii showed a 20–25% similarity of surface antigens. B. denticola was antigenically related to the B. intermedius and B. melaninogenicus strains by 10–15%. The remaining cross-reactivities were generally less than 5% among the Bacteroides species. The findings are consistent with specific surface antigenic determinants on the oral Bacteroides spp. and suggest the ability to detect specific responses to these organisms in periodontal disease patients.